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A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

A Bioluminescent and Fluorescent Orthotopic Syngeneic Murine Model of Androgen-dependent and Castration-resistant Prostate Cancer

Published on: March 6, 2018

[Molecular biology of castration resistant prostate cancer.]

Rafael Antonio Medina-López¹, Miquel Tarón², Ignacio Osman-García¹

¹Unidad de Gestión Clínica de Urología/Nefrología. Hospital Universitario Virgen del Rocío. Instituto de Biomedicina de Sevilla (IBIS). CSIC. Universidad de Sevilla. Sevilla. España.

Archivos Espanoles De Urologia

|October 16, 2018

Abstract

Objectives:

Castration resistant prostate cancer (CRPC) is an heterogeneous disease the molecular basis of which we are starting to know in depth. Currently, there are various pathways and targets under study, and probably many others to be characterized. In this paper, we review the most recent knowledge concerning the molecular biology of CRPC with a special focus on the therapeutic application of this knowledge.

Methods:

We performed a bibliographic review using PUBMED as the search engine, including the following terms: "Castration resistant prostate cancer", "genomics", "molecular biology", "AR", "WNT", "mTOR", "PTEN", "cell-cycle", "DNA damage repair gene"and "chromatin modifier genes".

Results:

CRPC has a high load of genetic alterations, probably derived from therapeutic pressure. The most frequent alterations involve the androgen receptor (RA) [60-70%] and the PI3K- AKT-mTOR [40-60%], even though other relevant pathways alterations have been identified such as those relative to cellular cycle [25%], DNA lesion repair genes [20%] and other pathway like WNT-βcatenin [15-22%]. The knowledge of these pathways is helping as a base for development of new therapeutic targets with promising results and multiple ongoing studies.

Conclusions:

Over the last decade, the progress in the knowledge of the molecular bases of CRPC has been very relevant. Even though AR alterations are the most frequent and best characterized, anomalies in other pathways have been also identified as important in the biology of CRPC and derived a notable therapeutic development.

Insights

Castration resistant prostate cancer (CRPC) involves frequent genetic alterations in androgen receptor (AR) and PI3K-AKT-mTOR pathways. Understanding these molecular changes drives new therapeutic target development for CRPC.

Area of Science:

Oncology
Molecular Biology
Genetics

Background:

Castration resistant prostate cancer (CRPC) is a complex disease with evolving molecular insights.
Therapeutic pressure contributes to a high frequency of genetic alterations in CRPC.

Purpose of the Study:

To review current knowledge on the molecular biology of CRPC.
To focus on the therapeutic applications of molecular insights in CRPC.

Main Methods:

Bibliographic review using PubMed.
Keywords included CRPC, genomics, molecular biology, AR, WNT, mTOR, PTEN, cell-cycle, DNA damage repair genes, and chromatin modifier genes.

Main Results:

Frequent alterations observed in CRPC: Androgen Receptor (AR) [60-70%], PI3K-AKT-mTOR [40-60%].
Other significant alterations include cell-cycle [25%], DNA repair genes [20%], and WNT-βcatenin [15-22%].
Knowledge of these pathways informs the development of novel therapeutic targets with promising ongoing studies.

Conclusions:

Significant progress in understanding CRPC molecular basis over the last decade.
While AR alterations are most common, other pathway anomalies are crucial for CRPC biology and therapeutic development.

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